ライフサイエンスコーパス: DLBCL

1 DLBCL and MCL had a poor prognosis (5-year DSS, 21% and

2 DLBCL exhibits highly aggressive and systemic progressio

3 ranscriptome sequencing in a cohort of 1,001 DLBCL patients to comprehensively define the landscape o

4 A historical retrospective cohort of 101 DLBCL/HCV-positive patients not undergoing AVT was enrol

5 ory de novo (n = 27) or transformed (n = 13) DLBCL.

6 ffuse large B-cell lymphoma (DLBCL; n = 34), DLBCL arising from chronic lymphocytic leukemia (Richter

7 ll response rate was 44% (MCL, 75%; FL, 38%; DLBCL, 18%).

8 We detected CagA expression in 20 of 42 DLBCL (MALT) cases (47.6%) and in 13 of 21 "pure" DLBCL

9 ented mature B-cell lymphoma consisting of 6 DLBCL and 1 FL.

10 MCL (57% [4 of 7]), DLBCL (56% [5 of 9]), and MF (88% [7 of 8]) were frequen

11 By CCC criteria, 6 of 8 DLBCL PDX models were B-cell receptor (BCR)-type tumors

12 -producing neutrophils infiltrated CXCL-8(+) DLBCL from both germinal center (GC) and non-GC subtypes

13 utic development in MYD88-mutated WM and ABC DLBCL, and possibly other diseases driven by mutated MYD

14 germinal center (GC) B-cell (GCB) DLBCL, ABC DLBCL cell lines expressed high levels of the AP-1 famil

15 the expression of nearly 3,000 genes in ABC DLBCL cells, and the chromatin surrounding many of these

16 hibitor AZD8835 showed marked potency in ABC DLBCL models, whereas the protein kinase B (AKT) inhibit

17 ion factor activator protein-1 (AP-1) in ABC DLBCL.

18 led to impaired growth of a majority of ABC DLBCL cell lines.

19 ortant element controlling the growth of ABC DLBCL.

20 ase signaling in mutated MYD88 WM and/or ABC DLBCL cells.

21 epresenting high-risk activated B-cell (ABC) DLBCL, while no response was observed in a third ABC mod

22 In addition, ABC-DLBCL frequently displays focal copy number gains affect

23 Although ABC-DLBCL has been associated with NF-kappaB activation, the

24 ibrutinib led to tumor regression in an ABC-DLBCL mouse model.

25 bservations raise the possibility for an ABC-DLBCL-specific resistance mechanism that is directed tow

26 combined venetoclax treatment of MCL and ABC-DLBCL xenografts with a pretargeted RIT (PRIT) system di

27 -cell (GCB-DLBCL), and activated B-cell (ABC-DLBCL) lymphomas.

28 Additionally, silencing p100 in ABC-DLBCL cells resulted in a GCB-like phenotype, with suppr

29 mutations are substantially enriched in ABC-DLBCL compared with germinal center B-cell DLBCL.

30 HOP to trigger oxidative stress and kill ABC-DLBCL cells in preclinical models.

31 o experiments revealed that MYD88-mutant ABC-DLBCL cells in particular display an actionable addictio

32 ect FOXP1 transcriptional enforcement of ABC-DLBCL hallmarks, including the classical NF-kappaB and M

33 ted a novel autochthonous mouse model of ABC-DLBCL that could be used as a preclinical platform for t

34 Specifically, in cell line models of ABC-DLBCL, Dox is often enriched in the cytoplasm away from

35 rapeutic approaches for the treatment of ABC-DLBCL.

36 ight be most effective in poor prognosis ABC-DLBCL, which shows higher levels of IL10RA, JAK2, and ST

37 their therapeutic efficacy for targeting ABC-DLBCL.

38 It is well documented that ABC-DLBCL cases have a significantly poorer survival respons

39 These findings indicate that ABC-DLBCL is a BCL6-dependent disease that can be targeted b

40 he proliferation of otherwise-unmodified ABC-DLBCL lines.

41 ified conserved pathways associated with ABC-DLBCL pathology.

42 In activated B cell DLBCLs (ABC-DLBCLs), a class of DLBCLs that respond poorly to curren

43 stasis to improve treatment outcomes for ABC-DLBCLs.

44 As a result, Dox-induced cytotoxicity in ABC-DLBCLs is often dependent on oxidative stress, rather th

45 (DeltaSUVmax), is for patients with advanced DLBCL, for whom iPET identifies patients with very good

46 enance as it is an oral drug, active against DLBCL that can be taken for years with an acceptable tox

47 Although DLBCL-associated CARD11 mutations in the caspase recruit

48 from a large cohort of primary human FL and DLBCL, we show a significant difference in the spectrum

49 ngle-agent dose for future studies in FL and DLBCL, with 800 mg being sufficient to consistently achi

50 Galpha13 and RhoA in Burkitt's lymphoma and DLBCL.

51 is the main outcome predictor, with MCL and DLBCL having a markedly poorer prognosis than EMZL and F

52 significantly better prognosis than MCL and DLBCL.

53 ell non-Hodgkin lymphoma: EMZL, FL, MCL, and DLBCL.

54 activation of specific NF-kappaB signals and DLBCL phenotype remain unclear.

55 patients who were resistant to R-CHOP, basal DLBCL mutations did not disappear from cfDNA.

56 n this study, we aimed at tracking the basal DLBCL genetic profile and its modification upon treatmen

57 Dual expresser MYC(+) BCL2(+) DLBCL defines a group at high risk of CNS relapse, indep

58 ession of established tumors in mice bearing DLBCL xenografts.

59 and HGBLs with features intermediate between DLBCL and Burkitt lymphoma into this new category.

60 provided insight into the potential of both DLBCL and FL cases to respond to agents targeting altera

61 tic factors in neuroblastoma, breast cancer, DLBCL, and medulloblastoma.

62 sight into the methylation changes of canine DLBCL, we investigated the DNA methylome in primary DLBC

63 C-DLBCL compared with germinal center B-cell DLBCL.

64 In activated B cell DLBCLs (ABC-DLBCLs), a class of DLBCLs that respond poor

65 AZD5363 induced apoptosis in PTEN-deficient DLBCLs irrespective of their molecular subtype.

66 itor AZD5363 was effective in PTEN-deficient DLBCLs through downregulation of the oncogenic transcrip

67 oles for p100 and p105 signaling in defining DLBCL molecular subtypes and posit MYD88/p100 signaling

68 imaging has an essential role in diagnosing DLBCL in the clinic; however, [(18)F]FDG-PET often faces

69 DNA from DLBCL patients correctly discovered DLBCL-associated mutations that were represented in >20%

70 and prevents the development of BCL6-driven DLBCL.

71 retreatment formalin-fixed paraffin-embedded DLBCL biopsies derived from patients subsequently treate

72 that inhibiting GCK may significantly extend DLBCL patient survival.

73 ts mainly of the lymphoma subtypes EMZL, FL, DLBCL, MCL, and MF.

74 sitive subjects, undergoing chemotherapy for DLBCL, were enrolled between June 2015 and December 2015

75 oxorubicin, vincristine, and prednisone) for DLBCL.

76 ncovered as a novel therapeutic strategy for DLBCL and BL treatment.

77 We have developed a PET imaging strategy for DLBCL that targets poly[ADP ribose] polymerase 1 (PARP1)

78 sequencing of pretreatment plasma cfDNA from DLBCL patients correctly discovered DLBCL-associated mut

79 CagA and CagA-signaling molecules in gastric DLBCL remains unexplored.

80 detected in the malignant B cells of gastric DLBCL, and the expression of these molecules is clinical

81 ients with stage IE/IIE1 HP-positive gastric DLBCL who received HPE as frontline treatment.

82 , and STAT3 but lower levels of BCL6 than GC-DLBCL and might be usefully combined with novel approach

83 ion of the XBP1-active form, compromised GCB DLBCL tumor growth in a mouse xenograft cancer model.

84 t IRE1-XBP1 downregulation distinguishes GCB DLBCL from other DLBCL subtypes and contributes to tumor

85 e expression profiles indicated that, in GCB DLBCL cancer samples, expression of IRE1 messenger RNA w

86 emonstrated to be recurrently mutated in GCB DLBCL; the transcriptional silencing of S1PR2 by FOXP1 r

87 ods After real-time determination of non-GCB DLBCL using the Hans immunohistochemistry algorithm, 206

88 prospectively enrolled patients with non-GCB DLBCL were more favorable than expected with R-CHOP and

89 83 patients with centrally confirmed non-GCB DLBCL who received one or more doses of study drug (91 R

90 TF3 expression was much higher in ABC vs GCB DLBCL cell lines.

91 -cell (ABC) and germinal center B-cell (GCB) DLBCL cell lines with aberrantly high FOXP1 levels; S1PR

92 ontrast to germinal center (GC) B-cell (GCB) DLBCL, ABC DLBCL cell lines expressed high levels of the

93 hat in the germinal center B-cell-like (GCB) DLBCL subtype, IRE1 expression is reduced to a level tha

94 models of germinal center B-cell like (GCB) DLBCL.

95 etter prognosis germinal center B-cell (GCB)-DLBCL subtype and is highly correlated with poor outcome

96 is an oncogenic biomarker of aggressive GCB-DLBCL.

97 ), germinal-center diffuse large B-cell (GCB-DLBCL), and activated B-cell (ABC-DLBCL) lymphomas.

98 f CD79A inhibited tonic BCR signaling in GCB-DLBCL lines but did not affect their calcium flux after

99 egions had no effect on BCR signaling in GCB-DLBCL lines, reflecting this subtype's exclusive use of

100 R signaling to proliferation and size of GCB-DLBCL lines, shown by the effect of BCR KO, was highly v

101 Despite the typically good outcomes of GCB-DLBCL, increased UCHL1 identifies a subgroup with early

102 KT, and forced activation of AKT rescued GCB-DLBCL lines from knockout (KO) of the BCR or 2 mediators

103 nificantly poorer survival response than GCB-DLBCLs in both the CHOP (cyclophosphamide, vincristine,

104 High-grade DLBCL and MCL, as well as MF, are frequently secondary e

105 e introduced a patient mutation into a human DLBCL cell line using CRISPR and deleted Crebbp and Ep30

106 f BCL2 Cross-validation experiments in human DLBCL samples revealed that both MYD88 and CD79B mutatio

107 Furthermore, analyses of human DLBCL genome sequencing data confirmed that BCL2 amplifi

108 ch testing for molecular features may impact DLBCL and FL management if clinical trials are designed

109 ensive analysis of global kinase activity in DLBCL, to identify novel therapeutic targets, and discov

110 mmunomodulatory agent, has shown activity in DLBCL.

111 not a requirement for cellular addiction in DLBCL.

112 ation for therapeutic response assessment in DLBCL.

113 dard chemotherapy drug, cyclophosphamide, in DLBCL cell lines.

114 High APRIL expression in DLBCL correlates with reduced patient survival, but the

115 onstrate that IKKbeta phosphorylates GLI1 in DLBCL.

116 de also significantly slowed tumor growth in DLBCL xenograft mice.

117 of which has been found to be much higher in DLBCL than in healthy tissues.

118 ll as new mechanisms of immunosuppression in DLBCL.

119 ive reviews the published studies on iPET in DLBCL, including the methods used to analyze iPET, its t

120 tected amplifications of the POU2F2 locus in DLBCL tumor biopsies and a recurrent mutation of threoni

121 ifferentiate inflammation from malignancy in DLBCL.

122 gest an important role of DNA methylation in DLBCL where aberrancies in transcription factors were fr

123 results explain the lack of ID mutations in DLBCL and reveal an unusual autoinhibitory domain struct

124 quencies of nonsense/frameshift mutations in DLBCL compared with FL.

125 e of CREBBP frameshift/nonsense mutations in DLBCL that result in loss of the protein, but may contra

126 CXCL-8 production in DLBCL was unrelated to the cell of origin, as APRIL-prod

127 s identified by gene expression profiling in DLBCL peripheral blood.

128 enetic drivers and their functional roles in DLBCL to identify new therapeutic opportunities in the d

129 apeutic inhibition of tonic BCR signaling in DLBCL.

130 he design of novel therapeutic strategies in DLBCL.

131 he superiority of an iPET-driven strategy in DLBCL.

132 mary, we identified expanded MDSC subsets in DLBCL, as well as new mechanisms of immunosuppression in

133 mechanisms of suppression of MDSC subsets in DLBCL.

134 Inhibition of SYK in DLBCL cells with tonic BCR signaling decreased phospho-A

135 hat GCK is a molecular therapeutic target in DLBCL tumors and that inhibiting GCK may significantly e

136 use as a biomarker and therapeutic target in DLBCL.

137 ival was greater in ophthalmic DLBCL than in DLBCL located outside the central nervous system and oph

138 ect is rooted in defective glycine uptake in DLBCL cell lines, rendering them uniquely dependent upon

139 esults in enhanced anti-lymphoma activity in DLBCLs.

140 btype-specific mechanisms of cytotoxicity in DLBCLs resulting from differences in the subcellular dis

141 e large B-cell lymphomas (DLBCLs), including DLBCLs with mucosa-associated lymphoid tissue (DLBCL[MAL

142 outcome compared with patients with ABC-like DLBCL without DE (5-year PFS rate, 39% [95% CI,19% to 59

143 rate and prolonged survival in the ABC-like DLBCL xenografts compared with the GCB-like DLBCL.

144 respect to COO (activated B-cell [ABC]-like DLBCL v germinal center B-cell [GCB]-like DLBCL) were ob

145 03) and compared with patients with GCB-like DLBCL without DE.

146 DLBCL xenografts compared with the GCB-like DLBCL.

147 ke DLBCL v germinal center B-cell [GCB]-like DLBCL) were observed in event-free survival, progression

148 3% [n = 20]), diffuse large B-cell lymphoma (DLBCL) (10% [n = 9]), mantle cell lymphoma (MCL) (8% [n

149 of 263]), and diffuse large B-cell lymphoma (DLBCL) (4.6% [12 of 263).

150 pregulated in diffuse large B-cell lymphoma (DLBCL) and can be targeted with the mTOR complex 1 (mTOR

151 erogeneity of diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) has been dramaticall

152 ios (SIRs) of diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) were calculated comp

153 y observed in diffuse large B cell lymphoma (DLBCL) and that disrupt ID-mediated autoinhibition, lead

154 e subtypes of diffuse large B-cell lymphoma (DLBCL) associated with poor outcomes after standard chem

155 to accelerate diffuse large B cell lymphoma (DLBCL) development and combinatorial targeting of these

156 Diffuse large B-cell lymphoma (DLBCL) has been categorized into two molecular subtypes

157 f BCL6-driven diffuse large B-cell lymphoma (DLBCL) in a murine model.

158 patients with diffuse large B-cell lymphoma (DLBCL) in first remission is important information for p

159 Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous disease defined by transcripti

160 patients with diffuse large B-cell lymphoma (DLBCL) is rituximab in combination with cyclophosphamide

161 Diffuse large B cell lymphoma (DLBCL) is the most common form of blood cancer and is ch

162 Diffuse large B-cell lymphoma (DLBCL) is the most common lymphoma in adults.

163 Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphom

164 Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphom

165 with relapsed diffuse large B-cell lymphoma (DLBCL) not eligible for autologous stem cell transplanta

166 llmark of the diffuse large B-cell lymphoma (DLBCL) of the activated B-cell (ABC) type, a molecular s

167 Primary diffuse large B-cell lymphoma (DLBCL) of the ocular region is rare, and the utility of

168 limited-stage diffuse large B-cell lymphoma (DLBCL) remains controversial.

169 r B-cell-like diffuse large B-cell lymphoma (DLBCL) represent the 2 major molecular DLBCL subtypes.

170 therapies for diffuse large B cell lymphoma (DLBCL) requires rapid assimilation of new biological dat

171 B cell (ABC) diffuse large B-cell lymphoma (DLBCL) subtype from the better prognosis germinal center

172 e majority of diffuse large B-cell lymphoma (DLBCL) tumors contain mutations in histone-modifying enz

173 wly diagnosed diffuse large B-cell lymphoma (DLBCL) underwent both FLT and FDG PET/CT 18-24 days afte

174 limited-stage diffuse large B-cell lymphoma (DLBCL) was shown in the Southwest Oncology Group (SWOG)

175 kitt (BL) and diffuse large B-cell lymphoma (DLBCL) xenografts blocked tumor growth, both when delive

176 ulloblastoma, diffuse large B-cell lymphoma (DLBCL), and EOC microarray gene expression datasets usin

177 lterations in diffuse large B-cell lymphoma (DLBCL), apart from translocations, has not been comprehe

178 C) subtype of diffuse large B cell lymphoma (DLBCL), engages the CARD11-MALT1-BCL10 (CBM) adapter com

179 In diffuse large B-cell lymphoma (DLBCL), the number of circulating monocytes and neutroph

180 e subtypes of diffuse large B cell lymphoma (DLBCL).

181 -2 (BCL2), in diffuse large B-cell lymphoma (DLBCL).

182 ns, including diffuse large B-cell lymphoma (DLBCL).

183 totoxicity in diffuse large B-cell lymphoma (DLBCL).

184 patients with diffuse large B-cell lymphoma (DLBCL).

185 treatment of diffuse large B-cell lymphoma (DLBCL).

186 impelling in diffuse large B-cell lymphoma (DLBCL).

187 sms including diffuse large B-cell lymphoma (DLBCL).

188 es, including diffuse large B-cell lymphoma (DLBCL).

189 subclasses of diffuse large B-cell lymphoma (DLBCL).

190 lymphoma and diffuse large B-cell lymphoma (DLBCL).

191 on feature of diffuse large B-cell lymphoma (DLBCL).

192 ike (non-GCB) diffuse large B-cell lymphoma (DLBCL).

193 cell lines of diffuse large B-cell lymphoma (DLBCL).

194 is pathway in diffuse large B-cell lymphoma (DLBCL).

195 homa (FL) and diffuse large B-cell lymphoma (DLBCL).

196 MYD88(L265P) diffuse large B-cell lymphoma (DLBCL).

197 in high-risk diffuse large B-cell lymphoma (DLBCL).

198 patients with diffuse large B-cell lymphoma (DLBCL).

199 (FL; n = 29), diffuse large B-cell lymphoma (DLBCL; n = 34), DLBCL arising from chronic lymphocytic l

200 erization of diffuse large B cell lymphomas (DLBCL), including large-scale exome capture, transcripto

201 a subset of diffuse large B-cell lymphomas (DLBCLs) and HGBLs with features intermediate between DLB

202 tage gastric diffuse large B-cell lymphomas (DLBCLs), including DLBCLs with mucosa-associated lymphoi

203 ffering from diffuse large B-cell lymphomas (DLBCLs).

204 ng the tumor-promoting factor APRIL mediates DLBCL progression.

205 homa (DLBCL) represent the 2 major molecular DLBCL subtypes.

206 was 6 months (MCL, 14 months; FL, 11 months; DLBCL, 1 month).

207 CREBBP-mutant DLBCL clones exhibited reduced histone H3 acetylation, e

208 ne expression classifiers identified two new DLBCL categories characterized by selective p100 (NF-kap

209 36 (78%) of 46 patients had de novo DLBCL and ten (22%) of 46 patients had transformed DLBCL

210 and high-resolution SNP array in 347 de novo DLBCL cases treated with R-CHOP (rituximab, cyclophospha

211 Restricting FISH analysis to the 10% of DLBCL patients who have a germinal center B-cell phenoty

212 OP) chemotherapy showed a rapid clearance of DLBCL mutations from cfDNA among responding patients.

213 ly R-CHOP-treated population-based cohort of DLBCL.

214 port is a targetable metabolic deficiency of DLBCL.

215 In a significant fraction of DLBCL patients, tumor cells constitutively produced the

216 results demonstrate that cfDNA genotyping of DLBCL is as accurate as genotyping of the diagnostic bio

217 the genetic and functional heterogeneity of DLBCL are urgently needed.

218 ource of tumor DNA for the identification of DLBCL mutations, clonal evolution, and genetic mechanism

219 ddress topical issues at the intersection of DLBCL biology and the clinic.

220 r predictive biomarkers in the management of DLBCL, such as the COO, within prospective clinical tria

221 hed and characterized faithful PDX models of DLBCL and demonstrated their usefulness in functional an

222 protein expression in preclinical models of DLBCL.

223 and correlates with response and outcome of DLBCL patients.

224 provides the first comprehensive overview of DLBCL biology and the basis for future precision medicin

225 coexpression as the most robust predictor of DLBCL outcome, and discuss rationally conceived experime

226 was correlated with a poor survival rate of DLBCL patients.

227 e in patients with chemosensitive relapse of DLBCL not eligible for ASCT or having relapse after ASCT

228 in patients with chemo-sensitive relapse of DLBCL who are not eligible for ASCT or who had relapse a

229 ese genes using an unbiased CRISPR screen of DLBCL cell lines to define oncogenes that promote cell g

230 we discuss how the molecular similarities of DLBCL and FL have provided insight into the potential of

231 activation and growth of the ABC subtype of DLBCL cell lines in vitro at high concentrations but sho

232 uld be efficacious in both major subtypes of DLBCL while avoiding systemic toxicity.

233 evaluate whether DAA antiviral treatment of DLBCL/HCV-infected patients in concomitance with chemoth

234 vated B cell DLBCLs (ABC-DLBCLs), a class of DLBCLs that respond poorly to current therapies, chromos

235 pient HLA mismatch and recipient HLA type on DLBCL risk are not well established.

236 d overall survival was greater in ophthalmic DLBCL than in DLBCL located outside the central nervous

237 alysis included 396 patients with ophthalmic DLBCL from January 1, 1973, through December 31, 2014, u

238 egulation distinguishes GCB DLBCL from other DLBCL subtypes and contributes to tumor growth.

239 correlated with FOXP1 expression in primary DLBCL accurately segregated the corresponding clinical s

240 CI, 63.2-104.8 months) than that in primary DLBCL that occurred outside the central nervous system a

241 inical subtypes of a large cohort of primary DLBCL isolates and identified conserved pathways associa

242 All patients diagnosed with primary DLBCL of the eye or retina (PVRL) or the eyelid, conjunc

243 we investigated the DNA methylome in primary DLBCLs in comparison with control lymph nodes by genome-

244 In primary DLBCLs, FOXO1 expression was present in 80% of tumors, c

245 (MALT) cases (47.6%) and in 13 of 21 "pure" DLBCL cases (61.9%).

246 oid tissue (DLBCL[MALT]) and without ("pure" DLBCL) the features of MALT lymphomas, can achieve long-

247 COO profiling in two prospective randomized DLBCL trials failed to identify prognostic subgroups, wh

248 ded samples from two prospective, randomized DLBCL trials (RICOVER-60, prospective, randomized study

249 s, those with zero or 1 mismatch had reduced DLBCL risk, (zero: IRR, 0.76, 95% confidence interval [9

250 Patients with chemotherapy-sensitive rel/ref DLBCL who underwent ASCT at two institutions and in whom

251 us on ASCT outcomes in patients with rel/ref DLBCL.

252 outcomes after ASCT in patients with rel/ref DLBCL.

253 ylaxis, in patients with relapsed/refractory DLBCL.

254 e outcome data from patients with refractory DLBCL are limited.

255 aluated outcomes in patients with refractory DLBCL which, for this study, was defined as progressive

256 For patients with refractory DLBCL, the objective response rate was 26% (complete res

257 for a population of patients with refractory DLBCL.

258 ose in patients with refractory and relapsed DLBCL in particular, is ongoing.

259 ombination therapy for a subset of high-risk DLBCL patients.

260 of immune checkpoint inhibitors in selected DLBCL subsets, and the potential activity of alternative

261 A subset of patients with limited-stage DLBCL randomly assigned to CHOP8 (n = 150) or CHOP3RT (n

262 arly analysis in patients with limited-stage DLBCL receiving CHOP3RT versus CHOP8, extended survival

263 rial in patients with nonbulky limited-stage DLBCL to evaluate the benefit of RT after rituximab plus

264 y RT in patients with nonbulky limited-stage DLBCL.

265 and possible unique biology of limited-stage DLBCL.

266 In a syngeneic DLBCL mouse model, this PARP1-targeted PET imaging appro

267 stic MR pairs induced loss of viability in t-DLBCL cells.

268 m cells were mostly affected suggesting that DLBCL shares a stem cell-like epigenetic pattern.

269 We address strategies to modulate the DLBCL microenvironment, including the use of immune chec

270 t increased FOXO1 activity is toxic to these DLBCL cells.

271 BCLs with mucosa-associated lymphoid tissue (DLBCL[MALT]) and without ("pure" DLBCL) the features of

272 atients (7.6%) developed a transformation to DLBCL.

273 and ten (22%) of 46 patients had transformed DLBCL.

274 -negative adults with de novo or transformed DLBCL and relapsed disease responsive to conventional ri

275 Results The 5-year post-treatment DLBCL survival was inferior to survival in the matched g

276 ed B-cell or non-germinal center B-cell type DLBCL also had an increased risk of CNS relapse.

277 Methods Patients with previously untreated DLBCL or other aggressive B-cell lymphoma were 60 to 80

278 puted tomography in 108 previously untreated DLBCL patients who received four 375 mg/m(2) rituximab i

279 ymphoma (PVRL) and ocular adnexal (OA)-uveal DLBCL.

280 %] and 23 men [48.9%]) and 349 with OA-uveal DLBCL (192 women [55.0%] and 157 men [45.0%]) had a simi

281 ; 95% CI, 14.2-61.8 months) than in OA-uveal DLBCL (96.0 months; 95% CI, 67.3-124.7 months; Mantel-Co

282 The 5-year survival in PVRL vs OA-uveal DLBCL differed by 17.7%, and overall survival was greate

283 41.4% (SE, 8.6%); among those with OA-uveal DLBCL, 59.1% (SE, 2.8%; Mantel-Cox test, P = .007).

284 For all PVRL and OA-uveal DLBCL, a Cox proportional hazards regression model affir

285 ith external beam radiation therapy, whereas DLBCL, MCL, and high Ann Arbor stage EMZL and FL were fr

286 es between 1987 and 2010, including 902 with DLBCL.

287 phoma Registry who were newly diagnosed with DLBCL between 2003 and 2011 were included in this study.

288 normalization of survival for patients with DLBCL achieving pEFS24, the estimated loss of residual l

289 Close to 90% of patients with DLBCL belong to the low- and intermediate-risk groups an

290 as to evaluate the survival of patients with DLBCL in remission compared with a matched general popul

291 combination with R-CHOP-21 for patients with DLBCL is safe.

292 ther it impacts the outcome of patients with DLBCL is unknown.

293 s can be used to risk-stratify patients with DLBCL treated with immunochemotherapy.

294 herapy with placebo in elderly patients with DLBCL who achieved a complete response (CR) or partial r

295 ble for increased mortality in patients with DLBCL.

296 antly prolonged PFS in elderly patients with DLBCL.

297 g able to predict survival for patients with DLBCL.

298 gs as maintenance in high-risk patients with DLBCL.

299 h 30, 2016), and none had had a relapse with DLBCL.

300 nts had stable disease, including those with DLBCL, Hodgkin's lymphoma, and multiple myeloma.